Rhabdomyosarcomas utilize developmental, myogenic growth factors for disease advantage: A report from the children's oncology group

Blandford, Mary; Barr, Frederic G.; Lynch, James C.; Randall, R. Lor; Qualman, Stephen J.; Keller, Charles

doi:10.1002/pbc.20466

Cited by 59 publications

(71 citation statements)

References 41 publications

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“…It has also been reported that both VEGF and PDGF families are involved in neo-angiogenesis in embryos and tumors (84). RMSs have been reported to express IGF and PDGF receptors (6). However, receptor expression is independent of signal molecule expression.…”

Section: Cytokine/cytokine Interactionsmentioning

confidence: 99%

“…However, receptor expression is independent of signal molecule expression. The expression of PDGF has been associated with poor prognosis (6). MET is the receptor of the hepatocyte growth factor (produced by bone marrow stromal cells) (85) specific for the acute phase of T-ALL (86).…”

Section: Cytokine/cytokine Interactionsmentioning

confidence: 99%

“…Other studies have reported the common appearance of antigens in Ewing's sarcoma/primitive neuroectodermal tumor (EWS/PNET) with lymphoblastic lymphoma (5). Rhabdomyosarcoma (RMS) belongs to the PNET family of tumors, which utilize embryonic genes for their progression (6). Acute lymphoblastic leukemia (ALL), which originates from the lymphoblast, also uses embryonic mechanisms for its differentiation and progression.…”

Section: Introductionmentioning

confidence: 99%

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Pathway simulations in common oncogenic drivers of leukemic and rhabdomyosarcoma cells: A systems biology approach

et al. 2012

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Abstract. A part of current research has intensively been focused on the proliferation and metabolic processes governing biological systems. Since the advent of high throughput methodologies such as microarrays, the load of genomic data has increased geometrically and along with that the need for computational methods to interpret these data. In the present study, we investigated in vitro the common proliferation and metabolic processes, associated with common oncogenic pathways, as far as gene expression is concerned, between the T-cell acute lymphoblastic leukemia (CCRF-CEM) and the rhabdomyosarcoma (TE-671) cell lines. We present a computational approach, using cDNA microarrays, in order to identify commonalities between diverse biological systems. Our analysis predicted that JAK1, STAT1, PIAS2 and CDK4 are the driving forces in the two cell lines. This type of analysis may lead to the understanding of the common mechanisms that transform physiological cells to malignant, and may reveal a new holistic approach to understanding the dynamics of tumor onset as well as the mechanistics behind oncogenic drivers. IntroductionIt is a fact that tumors can be as diverse as the patients carrying them. Due to these differences, tumors are extremely difficult to cure, as the effects of treatments differ depending on the patient. Previously, Nicolis showed that stem cells are found in different tumor types, suggesting that they can be the etiology of tumor maintenance and growth (1). However, there is evidence that even normal, already differentiated cells can be transformed into tumorigenic ones (1). Perilongo et al also reported a case of a child manifesting five different tumor types simultaneously (2). It may be possible that stem cells originating from the same organism possess similar mutations or alterations, thus giving rise to five different tumor types. Therefore, there is a need for the investigation of common pathways between different tumor types. The discovery of similar or opposite gene expression profiles could lead us to the understanding of a common tumor origin, if such exists.A number of studies have investigated the detection of cancer germ line genes (CGGs) both in pediatric sarcomas (3) and pediatric brain tumors (4). The discovery of global antigens for tumor vaccines could become salvatory for childhood malignancies (3). Other studies have reported the common appearance of antigens in Ewing's sarcoma/primitive neuroectodermal tumor (EWS/PNET) with lymphoblastic lymphoma (5). Rhabdomyosarcoma (RMS) belongs to the PNET family of tumors, which utilize embryonic genes for their progression (6). Acute lymphoblastic leukemia (ALL), which originates from the lymphoblast, also uses embryonic mechanisms for its differentiation and progression.Another point which requires attention is the regulation of genes through transcription factors (TFs). Knowledge of gene regulatory networks is considered to be of crucial importance for understanding diseases such as cancer, and may lead to new therapeutic approaches...

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Section: Cytokine/cytokine Interactionsmentioning

confidence: 99%

Section: Cytokine/cytokine Interactionsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Pathway simulations in common oncogenic drivers of leukemic and rhabdomyosarcoma cells: A systems biology approach

et al. 2012

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“…16 One group evaluated platelet-derived growth factor receptor (PDGFR) gene expression in pediatric rhabdomyosarcoma and demonstrated decreased failure-free survival for patients with tumors that overexpressed either PDGFR-a or PDGFR-b mRNA. 17 Several mediators of extracellular matrix breakdown have been shown to correlate with prognosis in patients with soft-tissue sarcoma. Increased levels of matrix metalloproteinase-2 (MMP-2), MMP-9, and urokinase plasminogen activator appear to confer a worse prognosis, whereas increased levels of tissue inhibitor of metalloproteinase-2 (TIMP-2) are associated with improved outcomes.…”

Section: Soft-tissue Sarcomamentioning

confidence: 99%

Markers of angiogenesis and clinical features in patients with sarcoma

DuBois

Demetri

2007

Cancer

129

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Objective: Patient outcome after traumatic brain injury (TBI) is highly variable. The underlying pathophysiology of this is poorly understood, but inflammation is potentially an important factor. Microglia orchestrate many aspects of this response. Their activation can be studied in vivo using the positron emission tomography (PET) ligand [11C](R)PK11195 (PK). In this study, we investigate whether an inflammatory response to TBI persists, and whether this response relates to structural brain abnormalities and cognitive function. Methods: Ten patients, studied at least 11 months after moderate to severe TBI, underwent PK PET and structural magnetic resonance imaging (including diffusion tensor imaging). PK binding potentials were calculated in and around the site of focal brain damage, and in selected distant and subcortical brain regions. Standardized neuropsychological tests were administered. Results: PK binding was significantly raised in the thalami, putamen, occipital cortices, and posterior limb of the internal capsules after TBI. There was no increase in PK binding at the original site of focal brain injury. High PK binding in the thalamus was associated with more severe cognitive impairment, although binding was not correlated with either the time since the injury or the extent of structural brain damage. Interpretation: We demonstrate that increased microglial activation can be present up to 17 years after TBI. This suggests that TBI triggers a chronic inflammatory response particularly in subcortical regions. This highlights the importance of considering the response to TBI as evolving over time and suggests interventions may be beneficial for longer intervals after trauma than previously assumed. ANN NEUROL 2011;

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“…Hh signaling is known to regulate multiple aspects of normal myogenesis, including the initiation and maintenance of MyoD family expression, the development, survival and proliferation of the epaxial and hypaxial muscle lineages, and the selection of muscle fiber type (Munsterberg et al, 1995;Borycki et al, 1999;Kruger et al, 2001). Moreover, elevated Hh signaling has recently been observed in sporadic cases of embryonal rhabdomyosarcoma (Blandford et al, 2006;Tostar et al, 2006), in addition to the rhabdomyosarcoma formation that is associated with Ptch1 haploinsufficiency. However, a precise mechanistic understanding of how the Hh signal modulates normal skeletal muscle development and promotes rhabdomyosarcoma formation does not exist.…”

Section: Introductionmentioning

confidence: 99%

The hedgehog regulated oncogenes Gli1 and Gli2 block myoblast differentiation by inhibiting MyoD-mediated transcriptional activation

et al. 2006

Oncogene

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Rhabdomyosarcomas utilize developmental, myogenic growth factors for disease advantage: A report from the children's oncology group

Abstract: Increased transcriptional levels of PDGF receptors and insulin-like growth factor are associated with decreased survival in rhabdomyosarcomas. Dual blockade of these growth-factor-signaling pathways may be a valuable strategy in preclinical therapeutic studies.

Cited by 59 publications

References 41 publications

Pathway simulations in common oncogenic drivers of leukemic and rhabdomyosarcoma cells: A systems biology approach

Pathway simulations in common oncogenic drivers of leukemic and rhabdomyosarcoma cells: A systems biology approach

Markers of angiogenesis and clinical features in patients with sarcoma

The hedgehog regulated oncogenes Gli1 and Gli2 block myoblast differentiation by inhibiting MyoD-mediated transcriptional activation

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